Atrial fibrillation in mitral stenosis.
Atrial fibrillation in itself is not life threatening. The prognosis is usually relatively favorable, even considering the risk of arterial thromboembolism. About 10% of patients develop heart failure. Mortality of patients with atrial fibrillation is 1.5-1.9 times higher than mortality in the population as a whole.
For the treatment of patients with atrial fibrillation, it is recommended to first translate the tachyarrhythmic form of blink into normal arrhythmic with the help of drugs (for example, cardiac glycosides, verapamil, beta-adrenergic receptor blockers) and at the same time to prescribe anticoagulant therapy. Then it is necessary to clarify the cause of atrial fibrillation and, depending on this cause (for example, valve defect or hyperthyroidism), to perform a surgical intervention or to select a medical therapy.
In the absence of a reason that can be directly affected, the patient’s data should be discussed in order to present what the prospects for drug or electrical cardioversion are and how appropriate they are. This primarily depends on how long the atrial fibrillation lasts (for example, less than 6 months or more than this period), how much the LP is increased (for example, does its diameter exceed 50 mm or is it less than 50 mm) and does flicker manifest Atrial clinical symptoms.
If you intend to perform cardioversion, then for 3 weeks. before the proposed date of this treatment procedure, the patient is prescribed anticoagulants and, only after achieving effective hypocoagulation, they proceed to medication (using flecainide, etacizin, propafenone, beta-adrenergic receptor blockers, cardiac glycosides, amiodarone, and new drugs of dronedarone or vernacalanta) or an electric cardiac glycoside, amiodarone, and new drugs of dronedarone or vernacalanta or an electric cardonic glucoside, amiodarone, and new dronedarone or vernacalanta treatment. Additionally prescribe drugs that stabilize the rhythm of heart contractions.
Patients whose rhythm disturbance is asymptomatic, elderly patients, as well as those for whom, based on the above criteria, cardioversion seems to have little promise, after long-term anticoagulant therapy should be treated only with heart rhythm-stabilizing drugs, in particular beta-adrenergic receptor blockers or cardiac glycosides.
Patients with clinical manifestations of atrial fibrillation, resistant to drug or electrical cardioversion, can be X-ray-surgical isolation of the orifices of the pulmonary veins by radiofrequency ablation or cryodestruction. Successful results after such interventions are observed in 70% of patients.
The auricle of the left atrium (LP) is the most frequent site of the formation of blood clots, which become the source of thromboembolism. Recently, a new method of treatment has been developed, which made it possible to reduce the risk of thromboembolism in patients with atrial fibrillation, which can be used especially in cases where the administration of anticoagulant therapy is contraindicated. With this method of treatment, which is abbreviated as PLAATO, the ear of the brain is isolated from its cavity by implanting an umbrella-like device into the atrium using catheter technology.
The following 3 forms of atrial fibrillation are distinguished:
• paroxysmal: duration not more than 2 days, spontaneous cessation of an attack;
• persistent: duration exceeds 7 days, arrhythmia can be eliminated;
• permanent: lasting more than one year, usually not stopped.
Atrial fibrillation associated with vagotonia usually appears at night or at rest, while with sympathicotonia, atrial fibrillation appears as a result of physical or psycho-emotional stress.
Atrial fibrillation is usually caused by an organic lesion of the heart, for example, ischemic heart disease, hypertension, mitral stenosis or mitral insufficiency, dilated or hypertrophic cardiomyopathy. There are also cases of idiopathic atrial fibrillation (atrial fibrillation, in 15% of cases). Patients with atrial fibrillation often complain of palpitations, a feeling of lack of air, interruptions in the work of the heart, and general weakness.
From a pathophysiological point of view, the occurrence of atrial fibrillation can be explained as follows. Flicker usually occurs in the PL, in particular due to the focal trigger activity of the atrium wall near the mouths of the pulmonary veins. Multiple paths of re-entry of excitation waves lead to arrhythmias, electrical tissue restructuring and structural changes. As a result, the atria lose their ability to contract and expand.
Blood stasis in the enlarged and non-contractile left atrium (LP) increases the risk of thromboembolism by 5-7 times compared with the risk of this complication in the population. Thromboembolism occurs in 20% of patients with atrial fibrillation, and in 80% of cases thromboembolism of cerebral arteries is observed. To reduce the risk of this complication, patients with atrial fibrillation are prescribed anticoagulants.
Signs of atrial fibrillation on ECG
Normal P teeth are not identified, fibrillation waves are seen, having different configurations.
Due to the chaotic conduct of excitation from the atria to the ventricles, a picture of absolute arrhythmia is noted.
Atrial fibrillation is the most frequent heart rhythm disorder requiring treatment. It usually appears in IHD, AH, mitral heart disease and hyperthyroidism.
The treatment is carried out with anticoagulants and antiarrhythmic drugs, electrical cardioversion, and only in the absence of the effect of these funds is shown catheter ablation of the pathways in the mouth of the pulmonary veins.
Atrial fibrillation is the most frequent heart rhythm disorder requiring treatment. In recent years, new data on the pathogenesis of atrial fibrillation have been accumulated, new methods of diagnosing and especially treating this disease have been developed.
Atrial fibrillation is observed in 1% of the adult population. In Germany, patients with atrial fibrillation are 1 million. With increasing age, especially after 80 years, the frequency of atrial fibrillation increases, reaching 10-16%.
When atrial fibrillation occurs, the occurrence of arousal is completely disturbed, the sinus rhythm disappears, and the normal R-wave stops registering on the ECG. Instead, so-called flicker waves (f) are registered, randomly following each other. Flicker waves are very small and sometimes inexperienced remain unnoticed. The frequency of flicker waves is 350-600 per minute. They are characterized by inconstancy of shape and size, and sometimes they are not even separated from each other.
Atrial fibrillation waves are conducted to the ventricles without any pattern, so the RR interval is irregular, which suggests an absolute arrhythmia. Usually the waves f are most clearly visible in leads II and / or V). The QRS complex, as a rule, is not wide, there are no pathological changes in the ST interval at first.
If the frequency of ventricular contractions in atrial fibrillation does not exceed 60 per minute, they speak of bradyarrhythmic flicker, but if it is more than 100 beats per minute, then it is tachyarrhythmic. In these cases, treatment is necessary.
ECG in sinus tachycardia of the heart
Sinus tachycardia is defined as sinus rhythm with a frequency higher than 100 beats / min. The cause of sinus tachycardia may be physical exertion, emotional stress, or any other condition leading to the activation of the sympathetic nervous system.
Sometimes sinus tachycardia may be inadequate. A possible cause is hyperthyroidism, but often the cause remains unclear. Most often this is observed in young women. A high heart rate is usually constant and shows an additional excess increase in response to physical exertion arising immediately after its onset.
Less commonly, inadequate sinus tachycardia occurs as a result of primary disturbances in the sinus node itself (re-entree of the sinus node).
Since sinus tachycardia is usually a physiological response, it rarely needs special treatment. However, if sinus tachycardia is inadequate, the heart rate can be reduced with the help of BAB or ivabradine, which is a selective inhibitor of the automatic function of the sinus node.
If the patient does not have a serious disease, then the heart rate at rest rarely exceeds 100 beats / min. Therefore, when detecting apparent sinus tachycardia at rest, the likelihood of a different heart rhythm, such as atrial tachycardia or atrial flutter (TP), should be considered.
Signs of reciprocal AV-node tachycardia on ECG
P teeth are layered on QRS complexes and therefore not visible. The QRS complex is narrow, the frequency of contractions of the ventricles is 150-200 per minute.
This form of supraventricular tachycardia occurs mainly in young people suffering from vascular dystonia. In people with heart disease, this form of heart rhythm disorder is quite rare.
The most common form of supraventricular tachycardia is reciprocal AV nodal tachycardia; A focus that initiates and maintains tachycardia is located above the level of the ventricles, in particular in the AV node.
It is believed that in the AV node, as a result of the so-called longitudinal dissociation, two pathways of excitation are formed: a slowly conducting, or alpha, path with a short refractory period and a fast conducting, or beta, with a long refractory period. Such splitting allows circular movement of the excitation wave when the excitation propagates from one path (alpha path) to another (beta path) and performs a fast circular motion.
At the analysis of an electrocardiogram the narrow QRS complexes, quickly following one after another, attract attention. The frequency of ventricular contractions is usually 120-220 per minute.
P teeth, although recorded, are negative and, due to the high frequency of contractions, are not visible or are not clearly visible. This results from the fact that teeth P are layered on the QRS complexes or are registered immediately after these complexes. The QRS and ST-T complexes do not initially change. Only with aberrant ventricular conduction, QRS complexes can be broadened, as in the blockade of the bundle of the His bundle (PG).
Accurately determining the boundaries of the P wave is sometimes difficult. Therefore, they used to speak simply about “supraventricular tachycardia”, making no distinction between atrial and AV-nodal tachycardia.
It is noteworthy that this tachycardia often occurs in young people, especially in girls, suddenly, for no apparent reason or after exercise, and also stops suddenly. These features have important clinical significance. Reciprocal AV-nodal tachycardia can also occur in patients with a heart condition. However, in most cases, the general condition of the patients, despite the rapid reduction of the ventricles, remains relatively satisfactory, since the blood pressure, as well as the stroke and minute volumes of the heart, decrease slightly.
It is known that after an attack of reciprocal AV-nodal tachycardia, there is often abundant urination due to the release of atrial natriuretic peptide.
Treatment of reciprocal AV-node tachycardia often begins with carotid sinus massage, the patient is asked to strain (Valsalva maneuver), give him cold water to drink, if necessary, intravenously, verapamil, cardiac glycosides, beta-adrenergic receptor blockers or flecainide, and if there is no effect from These measures address the issue of catheter ablation. Differential diagnosis and treatment of tachycardia with normal ventricular complexes are presented in the figure below.
Clinical manifestations of supraventricular tachycardias
Supraventricular tachycardia (SVT) can cause serious symptoms, such as syncopal or presynopal conditions (especially at the onset of an attack), marked palpitations, angina pectoris (even in the absence of coronary artery disease), shortness of breath, feeling of fatigue and polyuria due to the release of atrial natriuretic peptide.
Other patients may simply feel the arrhythmia without experiencing a pronounced heartbeat, or not feel any symptoms at all.
Patients may experience discomfort not only from symptoms caused by tachycardia, but also from the unpredictability of arrhythmias. Some people live in fear of waiting for the next attack and are afraid to travel or even leave the house for fear of a repetition of tachycardia.
In many patients, organic heart disease is absent, however, they fear that the arrhythmia may be a precursor of a severe heart attack or other serious cardiac catastrophe. It is necessary to convince these patients that they have “electrical” heart disease, and not circulatory disorders or structural cardiac pathology.
Stable supraventricular arrhythmia, occurring at a high frequency, can lead to the development of heart failure. In such cases, the term “tachycardiomyopathy” is used. At the same time, restoration of a normal rhythm is accompanied by regress of heart failure.
Sometimes in patients without coronary artery disease, tachycardia can lead to pronounced ECG changes characteristic of myocardial ischemia. It is well known that an increase in serum troponin levels is considered as a sign of acute MI.
However, a slight increase in troponin concentration can be observed in patients with a long-existing tachycardia, in whom angiography shows no signs of coronary disease or whose age and degree of coronary risk make the presence of coronary pathology unlikely. A slight increase in troponin levels in patients with supraventricular tachycardia (SVT) should not be considered a sign of MI.
ECG for reciprocal tachycardias from AV-connection (AVRT, AVURT)
There are two main types of supraventricular tachycardia (SVT): AV re-entry tachycardias with AV involvement and atrial tachyarrhythmias. (In the Russian-language literature for tachycardia, based on the re-entry mechanism, or “re-entry of the excitation wave”, the term “reciprocal tachycardia” is often used.)
When reciprocal tachycardias involving the AV connection between the atria and the ventricles, there is an additional electrical connection. In this case, the impulse can repeatedly and at high speed circulate between the atria and the ventricles in a circle consisting of a normal AV connection and an additional AV connection. As a rule, from the atria to the ventricles the impulse is conducted through the AV node, and then returns from the ventricles to the atria through an additional connection.
There are two types of additional connections between the atria and the ventricles.
Additional conductive path. In atrioventricular reciprocal (re-entree) tachycardia (AVRT), the additional connection is represented by a bundle of myocardial fibers, which, like a bridge, spreads through the atrioventricular sulcus and thus “bypasses” the AV node. If this additional AV route is able to conduct impulses from the atria to the ventricles, then the patient has WPW syndrome.
In atrioventricular nodal reciprocal (re-entree) tachycardia (AVRT), the AV node and the atrial tissue adjacent to it are functionally dissociated into fast and slow paths, so there are two pathways in the AV node itself. With this tachycardia, AV conduction from the atria to the ventricles is carried out along the slow path, and conduction from the ventricles to the atria through the rapid path.
Atrial tachyarrhythmias. The second group of supraventricular tachycardias (SVT) includes arrhythmias caused by frequent abnormal electrical activity within the atria: AF, TP, and atrial tachycardia. The mechanism underlying this type of tachycardia is limited to atrial tissue.
Unlike tachycardia of the first group, with atrial tachyarrhythmias, the AV node is not part of the mechanism of tachycardia, but only conducts (partially or fully) atrial impulses on the ventricles. Atrial tachyarrhythmias are often associated with diseases of the myocardium, valvular apparatus of the heart, or with extracardiac pathology, while reciprocal tachycardias involving AV compounds are due to the existence of abnormal electrical
Classification of supraventricular tachycardias (SVT)
Some tachycardias occur in the atria or the AV connection and, therefore, are supraventricular in origin. In this case, the ventricles are activated through the His-Purkinje fast-conducting system, as a result of which narrow ventricular complexes are usually formed. There are two main types of supraventricular tachycardias (SVT).
The first type is reciprocal tachycardias involving the AV connection. They involve an additional electrical connection between the atria and the ventricles.
In this case, the impulse can circulate repeatedly and at high speed between the atria and the ventricles in a circle consisting of a normal AV connection and an additional AV connection. As a rule, such tachycardia is not associated with any other pathology of the heart.
The second type is atrial tachyarrhythmias, due to frequent pathological electrical activity within the atria (ie, AF, TP, and atrial tachycardia). At the same time, the AV-node is not an integral part of the tachycardia mechanism, but only transmits (partially or completely) impulses from the atria to the ventricles. Tachycardias of this type are often associated with various heart diseases.
Some tachycardias occur in the atria or the AV connection and, therefore, are supraventricular in origin. All of them have one common feature: since they arise above the level of the bundle of the His branch, the ventricles are activated by impulses propagating through a specialized intraventricular rapidly conducting system, and therefore ventricular complexes are usually normal and narrow.
However, it is very important to realize and take into account that there are significant differences in the mechanisms of development, ECG signs and approaches to the treatment of various forms of supraventricular tachycardias (SVT). It is necessary to determine the type of tachycardia, and not just treat all tachycardias with narrow QRS complexes as supraventricular tachycardias (SVT).
The appearance of extrasystoles on an ECG in a teenager
Another predisposing factor to the appearance of extrasystoles on an adolescent ECG is an overload of the heart muscle during puberty. The fact is that different elements of the cardiovascular system develop at a given time at a different speed – as a rule, the heart grows much faster and more actively than blood vessels, which leads to an increase in blood pressure. This can be easily understood by imagining how a powerful pump tries to pump as much fluid as possible through a narrow opening. Increased load on the myocardium leads to increased excitability of its contractile elements, which facilitates the occurrence of extrasystoles. In adolescents with such a heart overload, extraordinary contractions are not observed at rest, but during exercise, the child may complain of heartbeat and interruptions in heart function. In addition, high blood pressure during this period can cause dizziness, headaches and flickering flies before the eyes. This state also disappears without a trace after puberty, when the work of the heart and the volume of the circulatory system begin to match each other.
If an adolescent 12-14 years old on an ECG, extrasystoles were found without other signs of organic heart damage (for example, congenital defects or consequences of a rheumatic attack), then such a child is simply sent for a second analysis after two weeks. If the conclusion “extrasystolic arrhythmia” is confirmed, then the adolescent is put on record in the cardiologic dispensary. There is nothing terrible in this, it just means that every six months the child will be examined by a cardiologist, moreover, such children are exempted from physical education, since physical exertion can provoke more severe heart rhythm disturbances. As a rule, after adolescence, the extrasystoles on the ECG disappear and the young person is removed from the register without consequences. If the arrhythmia remains unchanged, then they try to find its cause and begin drug therapy.
Although adolescents who have an irregular heartbeat, and require more careful medical attention, parents should treat this as part of the maturing of the young body, as a temporary condition that passes completely a couple of years. There is no specific treatment for this transient pathology, it is recommended only a high vitamin ration, especially rich in such vitamins as C and E – the main antioxidants of the body. It is also necessary to monitor the balance of inorganic ions, especially magnesium and potassium – in conditions and diseases accompanied by loss of fluid (taking diuretics, diarrhea, loss of electrolytes and sweat in hot weather) it is necessary to bring products rich in potassium (dried apricots, baked potatoes) into the diet and adequately compensate for the loss of minerals (for example, by taking Regidron solution in case of diarrhea). The lack of these ions in adolescents with extrasystoles and arrhythmias may result in more severe heart rhythm disturbances.
Extrasystoles on the ECG in a teenager – what is it and treatment recommendations
The most tireless organ of our body, no doubt, is the heart. It is reduced in the normal 60-70 times per minute, pumping huge amounts of blood. In view of the enormous importance of this organ, the work of the heart is regulated both from the outside (through the effect of hormones and the autonomic nervous system on the myocardium) and from the inside (the system of self-regulation and automatic heart function). However, this is also a kind of “Achilles’ heel” of the heart – sometimes these two systems work in isolation, leading to various heart rhythm disorders.
Many healthy children and adolescents in the period of 12-14 years for the first time go to a study such as electrocardiography – registration of changes in the electric field of the heart. This study is carried out as part of a routine medical examination, and often it records a heart rhythm disorder such as beats, an extraordinary, sudden contraction of the heart. Extrasystoles are the most common cause of arrhythmias in people of different ages. For many adolescents, this condition does not manifest itself with absolutely no symptoms, only a few note periodic interruptions in the work of the heart and heartbeat. Parents often start to panic when they see such an ECG conclusion, thinking that their child has a serious pathology. However, such results of electrocardiography in adolescence are quite common and temporary.
The heart of an adult and the heart of a child differ in many ways from each other, in addition to the size of the differences relate to the distribution of muscle mass and frequency of contractions. In adolescence, there is a rapid change in the entire cardiovascular system, the body matures and needs a different blood supply to the organ. Already these rapid changes in themselves lead to the emergence of extrasystoles – during the growth of the heart, special, excitable elements arise among its cells, capable for one reason or another to generate a nerve electrical impulse that causes a contraction of cardiomyocytes – myocardial cells. The structure of the myocardium, especially the fact that absolutely all cardiomyocytes are interconnected in a single three-dimensional network, therefore, the electrical impulse that has arisen in one place very quickly spreads to the whole heart and causes its contraction – this is the extrasystole. As a rule, after the end of adolescence and puberty, the excitable myocardial cells are already regulated by both intracardiac and intracardiac factors, so extrasystoles no longer arise.